Effect of axotomy along with hypoxia on the NADPH-d activity in the brainstem motor neurons of albino rats

J. Y. Shieh, H. M. Chang, J. H. Lue, C. Y. Wen

研究成果: 雜誌貢獻文章

1 引文 (Scopus)

摘要

Peripheral axotomy of the cranial nerves has been reported to induce expression of nitric oxide synthase (NOS) in the relative motor neurons. However, all of these studies were carried out in the normoxic environment, and in what manner would the intracellular enzyme activity express under hypoxia was still unclear. In the present study, we employed the nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry to label the NO-containing neurons in some brainstem motor nuclei after axotomy along with hypoxia in the rat. Either side of the vagal and hypoglossal nerves was transected in the same animal. Following axotomy, half of the animals were subjected to hypoxia by housing in the altitude chamber (about 380 torr). NADPH-d reaction was assessed at 3, 7, 14, 30 and 60 days post-axotomy. The results obtained from the present study revealed that the number of NADPH-d positive neurons peak at 14 days in the hypoglossal nucleus (HN). While in the dorsal motor nucleus of vagus (DMN) and nucleus ambiguus (NA), the number of NADPH-d positive neurons increased steadily with the time course. Besides, we also found that upregulation of the NADPH-d activity in the HN and DMN of hypoxic rats was more significant than normoxic ones, but this state of enzyme expression was not observed in the NA. The discrepancy of NADPH-d expression between DMN and NA under hypoxia treatment may result from different properties of embryonic origins. It is well known that O2 deprivation is one of the factors that can lead to poor cellular function. Thus, the higher expression of NADPH-d in motor neurons after axotomy along with hypoxia suggest that NO might play an important role in the mechanisms of the hypoxla-reiated neuropathogenesis.
原文英語
期刊FASEB Journal
12
發行號5
出版狀態已發佈 - 三月 20 1998
對外發佈Yes

指紋

Axotomy
NAD(P)H dehydrogenase (quinone)
Motor Neurons
brain stem
motor neurons
NADP
albino
NADP (coenzyme)
Brain Stem
Neurons
Rats
hypoxia
rats
Medulla Oblongata
neurons
nerve tissue
Animals
Hypoglossal Nerve
Cranial Nerves
Enzyme activity

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

引用此文

Effect of axotomy along with hypoxia on the NADPH-d activity in the brainstem motor neurons of albino rats. / Shieh, J. Y.; Chang, H. M.; Lue, J. H.; Wen, C. Y.

於: FASEB Journal, 卷 12, 編號 5, 20.03.1998.

研究成果: 雜誌貢獻文章

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abstract = "Peripheral axotomy of the cranial nerves has been reported to induce expression of nitric oxide synthase (NOS) in the relative motor neurons. However, all of these studies were carried out in the normoxic environment, and in what manner would the intracellular enzyme activity express under hypoxia was still unclear. In the present study, we employed the nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry to label the NO-containing neurons in some brainstem motor nuclei after axotomy along with hypoxia in the rat. Either side of the vagal and hypoglossal nerves was transected in the same animal. Following axotomy, half of the animals were subjected to hypoxia by housing in the altitude chamber (about 380 torr). NADPH-d reaction was assessed at 3, 7, 14, 30 and 60 days post-axotomy. The results obtained from the present study revealed that the number of NADPH-d positive neurons peak at 14 days in the hypoglossal nucleus (HN). While in the dorsal motor nucleus of vagus (DMN) and nucleus ambiguus (NA), the number of NADPH-d positive neurons increased steadily with the time course. Besides, we also found that upregulation of the NADPH-d activity in the HN and DMN of hypoxic rats was more significant than normoxic ones, but this state of enzyme expression was not observed in the NA. The discrepancy of NADPH-d expression between DMN and NA under hypoxia treatment may result from different properties of embryonic origins. It is well known that O2 deprivation is one of the factors that can lead to poor cellular function. Thus, the higher expression of NADPH-d in motor neurons after axotomy along with hypoxia suggest that NO might play an important role in the mechanisms of the hypoxla-reiated neuropathogenesis.",
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N2 - Peripheral axotomy of the cranial nerves has been reported to induce expression of nitric oxide synthase (NOS) in the relative motor neurons. However, all of these studies were carried out in the normoxic environment, and in what manner would the intracellular enzyme activity express under hypoxia was still unclear. In the present study, we employed the nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry to label the NO-containing neurons in some brainstem motor nuclei after axotomy along with hypoxia in the rat. Either side of the vagal and hypoglossal nerves was transected in the same animal. Following axotomy, half of the animals were subjected to hypoxia by housing in the altitude chamber (about 380 torr). NADPH-d reaction was assessed at 3, 7, 14, 30 and 60 days post-axotomy. The results obtained from the present study revealed that the number of NADPH-d positive neurons peak at 14 days in the hypoglossal nucleus (HN). While in the dorsal motor nucleus of vagus (DMN) and nucleus ambiguus (NA), the number of NADPH-d positive neurons increased steadily with the time course. Besides, we also found that upregulation of the NADPH-d activity in the HN and DMN of hypoxic rats was more significant than normoxic ones, but this state of enzyme expression was not observed in the NA. The discrepancy of NADPH-d expression between DMN and NA under hypoxia treatment may result from different properties of embryonic origins. It is well known that O2 deprivation is one of the factors that can lead to poor cellular function. Thus, the higher expression of NADPH-d in motor neurons after axotomy along with hypoxia suggest that NO might play an important role in the mechanisms of the hypoxla-reiated neuropathogenesis.

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